The pleiotropic cytokines, IL-1β and TNFα, among other effectors, have been implicated in the pathophysiology of asthma and other inflammatory diseases. Altered airway responsiveness to bronchoactive constrictor and relaxant stimuli is the characteristic pathophysiological feature of bronchial asthma. While infiltration of the airways with inflammatory cells, principally involving eosinophils, mast cells, and lymphocytes is characteristic of altered airway responsiveness, airway smooth muscle (ASM) itself has the capacity to autologously induce changes in its constrictor and relaxant responsiveness secondary to the induced release and autocrine actions of certain pro-inflammatory cytokines. For example, IgE-dependent atopic sensitization and rhinovirus inoculation of ASM provoke the release of Th1 and Th2-type cytokines, IL-1β, and other cytokines from the ASM itself; and these cytokines acting alone or in combination elicit changes in ASM responsiveness.
Effectors such as cytokines typically are involved in a broad class of signaling events. Indeed, altered levels in IL-1β, and TNFα signaling activity are observed in inflammatory diseases other than asthma as well.